中国病理生理杂志2024，Vol.40Issue(2)：230-237,8.DOI:10.3969/j.issn.1000-4718.2024.02.005
hsa-miR-204-5p对人脐静脉内皮细胞生物学行为的影响
Effects of hsa-miR-204-5p on biological behaviors of human umbilical vein endothelial cells
摘要
Abstract
AIM:This study aimed to investigate the effects of hsa-miR-204-5p on the viability,migration,cell cycle,and apoptosis of human vascular endothelial cells.METHODS:We established a model using the hsa-miR-204-5p mimic in the human umbilical vein endothelial cell line EA.hy926.We evaluated the effects of hsa-miR-204-5p on endothelial cell functionality through various analyses,including cell scratch,Transwell,CCK-8,cell cycle,and apopto-sis assays.Subsequently,we employed RNA sequencing and RT-qPCR to predict and verify the downstream target genes of hsa-miR-204-5p.Genes meeting the criteria of log2FC≤-0.5 and P＜0.05 in RNA sequencing and those predicted as downstream target genes of hsa-miR-204-5p by the miRWalk database were intersected.Furthermore,we conducted Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analyses.RESULTS:Overexpres-sion of hsa-miR-204-5p inhibited the viability and migration of EA.hy926 cells,and reduced their apoptotic rate and the proportion of cells in S phase.Enrichment analyses showed that downstream target genes of hsa-miR-204-5p,including MAPT,PPP3R1,PRKACB,PTPRR,MAP2K4,CACNA2D2 and RPS6KA6,exhibited enrichment in MAPK signaling pathway.RT-qPCR results revealed that the mRNA expression levels of MAPT and MAP2K4,especially MAPT,were sig-nificantly down-regulated after overexpression of hsa-miR-204-5p.CONCLUSION:The findings suggest that hsa-miR-204-5p suppresses the biological behaviors of endothelial cells,such as viability,migration,and apoptosis,likely through the inhibition of MAPT/MAPK signaling pathway.关键词
hsa-miR-204-5p/血管内皮细胞/RNA测序/MAPK信号通路Key words
hsa-miR-204-5p/vascular endothelial cells/RNA seqencing/MAPK signaling pathway分类
医药卫生引用本文复制引用
张义炜,杨英,潘尚领..hsa-miR-204-5p对人脐静脉内皮细胞生物学行为的影响[J].中国病理生理杂志,2024,40(2):230-237,8.基金项目
国家自然科学基金助项目(No.81960266) （No.81960266）
